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Year 2 Cardio > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

the cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult

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2
Q

What is haemostasis for?

A

Prevention of blood loss from intact vessels
Arrest bleeding from injured vessels
enable tissue repair

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3
Q

What are the stages of haemostasis?

A

Primary
Secondary
Fibrinolysis

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4
Q

What are the steps of haemostasis?

A

Vessel constriction
Formation of an unstable platelet plug
Stabilisation of plug with fibrin
Vessel repair and dissolution of clot

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5
Q

Why is it important to understand haemostatic mechanisms?

A

Diagnose and treat bleeding disorders

Control bleeding in individuals who do not have an underlying bleeding disorder

Identify risk factors for thrombosis

Treat thrombotic disorders

Monitor the drugs that are used to treat bleeding and thrombotic disorders

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6
Q

What is low platelets known as?

A

thrombocytopenia

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7
Q

What causes low platelets?

A

Bone marrow failure eg: leukaemia, B12 deficiency

Accelerated clearance eg: immune (ITP), Disseminated Intravascular Coagulation (DIC)

Pooling and destruction in an enlarged spleen

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8
Q

What causes impaired function of platelets?

A

Hereditary absence of glycoproteins or storage granules (rare)

Acquired due to drugs: aspirin, NSAIDs, clopidogrel (common)

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9
Q

What are conditions that impaired platelet function?

A

Glanzmann’s thrombasthenia
Bernard Soulier syndrome
Storage Pool diseas

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10
Q

What are the two functions of VWF?

A

Binding to collagen and capturing platelets
Stabilising Factor VIII
Factor VIII may be low if VWF is very low

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11
Q

What is VWD?

A

Von Willebrand disease
Hereditary decrease of quantity +/ function (common)
Acquired due to antibody (rare)

VWD is usually hereditary (autosomal inheritance pattern)
Deficiency of VWF (Type 1 or 3)
VWF with abnormal function (Type 2)

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12
Q

What is the third aspect that a defect in can affect haemostasis?

A

The vessel wall

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13
Q

What causes defects in the vessel wall?

A

Inherited (rare)

Hereditary haemorrhagic telangiectasia

Ehlers-Danlos syndrome

and other connective tissue disorders

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14
Q

What are the clinical features of primary haemostasis bleeding?

A

Immediate
Prolonged bleeding from cuts
Nose bleeds (epistaxis):prolonged > 20 mins
Gum bleeding: prolonged
Heavy menstrual bleeding (menorrhagia)
Bruising (ecchymosis), may be spontaneous/easy
Prolonged bleeding after trauma or surgery

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15
Q

What are petechia and purpura?

A

caused by bleeding under the skin

Purpura do not blanch when pressure is applied

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16
Q

What is a feature (to diagnose) of thrombocytopenia?

A

Petechia

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17
Q

What are tests for disorders of primary haemostasis?

A

Platelet count, platelet morphology

Bleeding time (PFA100 in lab)

Assays of von Willebrand Factor

Clinical observation

Note –coagulation screen (PT, APTT) is normal (except more severe VWD cases where FVIII is low)

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18
Q

What are the treatments if it is failure of production?

A 
Failure of production/function
Replace missing factor/platelets  e.g. VWF containing concentrates
 i) Prophylactic
ii) Therapeutic
Stop drugs e.g. aspirin/NSAIDs
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19
Q

What are treatments for immune destruction? (including ITP)

A

Immune destruction
Immunosuppression (e.g. prednisolone)
Splenectomy for ITP

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20
Q

What are treatments for increased consumption?

A

Treat cause

Replace as necessary

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21
Q

What are some additional haemostatic treatments?

A
  • Desmopressin (DDAVP)
    Vasopressin analogue
    2-5 fold increase in VWF (and FVIII)
    releases endogenous stores (so only useful in mild disorders)
  • Tranexamic acid
    Antifibrinolytic
  • Fibrin glue/spray
  • Other approaches e.g hormonal (oral contraceptive pill for menorrhagia)
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22
Q

What is the role of coagulation?

A

to generate thrombin (IIa), which will convert fibrinogen to fibrin

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23
Q

What would a deficiency in any coagulant factor cause?

A

Deficiency of any coagulation factor results in a failure of thrombin generation and hence fibrin formation

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24
Q

What are hereditary causes of coagulation factor production?

A

Factor VIII/IX: haemophilia A/B

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25
Q

What are acquired causes of disrupted coagulation factor production?

A

Liver disease
Anticoagulant drugs
Warfarin
Direct Oral Anticoagulants (DOACs)

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26
Q

What are acquired causes of dilution causing disorder of coagulation?

A

Blood transfusion

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27
Q

What are acquired causes of increased consumption?

A

Disseminated intravascular coagulation (DIC) – common

Immune – autoantibodies – rare

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28
Q

Wha are the features of inherited coagulation disorders?

A 
Haemophilia A (Factor VIII deficiency) 
Haemophilia B (Factor IX deficiency) 
 sex linked
1 in 104 births
Others are very rare (autosomal recessive)
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29
Q

What should be avoided in patients with haemophilia?

A

IM injections

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30
Q

Why are different coagulation factor deficiencies not all the same?

A

Factor VIII and IX (Haemophilia)
Severe but compatible with life
Spontaneous joint and muscle bleeding

Prothrombin (Factor II)
Lethal

Factor XI
Bleed after trauma but not spontaneously

Factor XII
No bleeding at all

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31
Q

Why does liver failure cause coagulation disorders?

A

Most coagulation factors are synthesised in the liver

32
Q

Why does dilution produce coagulation disorders?

A

Red cell transfusions no longer contain plasma

Major haemorrhage requires transfusion of plasma as well as red cells and platelets

33
Q

What are the features of increased consumption?

A

Generalised activation of coagulation – Tissue factor

Associated with sepsis, major tissue damage, inflammation

Consumes and depletes coagulation factors

Platelets consumed - thrombocytopenia

Activation of fibrinolysis depletes fibrinogen – raised D-dimer
(a breakdown product of fibrin)

Deposition of fibrin in vessels causes organ failure

34
Q

What are the clinical features of coagulation disoders?

A

superficial cuts do not bleed (platelets)
bruising is common, nosebleeds are rare
spontaneous bleeding is deep, into muscles and joints
bleeding after trauma may be delayed and is prolonged
Bleeding frequently restarts after stopping

35
Q

What are the tests for coagulation disorders?

A

Screening tests (‘clotting screen’)
Prothrombin time (PT)
Activated partial thromboplastin time (APTT)
Full blood count (platelets)

Coagulation factor assays (for Factor VIII etc)
Tests for inhibitors

36
Q

What are the different types of factor replacement therapy?

A

Fresh Frozen Plasma
Cryoprecipitate
Factor Concentrates
Recombinate forms of FVIII and FIX

37
Q

What are the features of FFP?

A

Contains all Coagulation factors

38
Q

What are the features of cryoprecipitate?

A

Rich in Fibrinogen, FVIII, VWF, Factor XIII

39
Q

What are the features of factor concentrates?

A

Concentrates available for all factors except factor V.

Prothrombin complex concentrates (PCCs) Factors II, VII, IX, X

40
Q

Wen are recombinant forms of FVIII and FIX used?

A

‘On Demand’ to treat bleeds

Prophylaxis to prevent bleeds

41
Q

How to disorders of thrombosis present?

A

Pulmonary embolism

Deep vein thrombosis

42
Q

What are the features of PE?

A 
Tachycardia
Hypoxia
Shortness of breath
Chest pain
Haemopysis
Sudden death
43
Q

What are the features of DVT?

A 
Painful leg
Swelling
Red
Warm
May embolise to lungs
Post thrombotic syndrome
44
Q

What type of thrombosis are PE and DVT?

A

Venouse

45
Q

What is thrombosis?

A 
Intravascular coagulation
Inappropriate coagulation
Venous (or arterial)
Obstructs flow
May embolise to lungs
46
Q

What is Virchow’s triad?

A 
Three contibutpry factors to thrombosis
Blood (dominant in venous)
Vessel wall (dominant in arterial)
Blood flow (both)
47
Q

What is thrombophilia?

A

Increased risk of thrombosis

48
Q

What is indicative of thrombosis?

A

Thrombosis at young age
‘spontaneous thrombosis’
Multiple thromboses
Thrombosis whilst anti-coagulated

49
Q

What are anticoagulant proteins?

A

Antithrombin
Protein C
Protein S

50
Q

What is the role of vessel wall in thrombosis?

A

We know little about the role of the vessel wall in venous thrombosis.
Many proteins active in coagulation are expressed on the surface of endothelial cells and their expression altered in inflammation (TM, EPCR, TF)

51
Q

What are the risk factors for venous thrombosis?

A

Age
Genetic
Environmental

52
Q

How to you prevent thrombosis?

A

Assess and prevent risks

Prophylactic anticoagulant therapy

53
Q

How do you reduce the risk of recurrence?

A

lower procoagulant factors
e.g.: warfarin, DOACs
increase anticoagulant activity
e.g: heparin

54
Q

When is therapeutic anticoagulation used?

A

Venous thrombosis
Initial treatment to minimise clot extension/embolisation (< 3 months)
Long term treatment to reduce risk of recurrence

Atrial fibrillation:
800 per 100 000 population potentially eligible in 1 year
To reduce risk of embolic stroke

Mechanical prosthetic heart valve

55
Q

When is thromboprophylaxis used?

A

following surgery, during hospital admission, during pregnancy

56
Q

What are the main features of heparin?

A

Naturally occurring glycosaminoglycan
Produced by mast cells of most species
Porcine products used in UK
Varying numbers of saccharides in chains – differing lengths
- Long chains - Unfractionated (UFH) – intravenous administration, short half life
- Low molecular weight (LMWH) – subcutaneous administration

57
Q

What are the actions of unfractionated heparin?

A

Enhancement of Antithrombin

Changing the active site of antithrombin

Far greater affinity for target proteases (FXa and thrombin)

Inactivation of thrombin (Hep binds AT + Thrombin)

Inactivation of FXa (Hep binds AT only)

(Inactivation of FIXa, FXIa, FXIIa)

58
Q

What is the action of low-molecular weight heparin?

A

Predominantly against FXa

Shorter chains are not long enough to wrap around thrombin and antithrombin

59
Q

What is the effect of unfractionated heparin on test?

A

Prolongation of APTT

60
Q

How does Warfarin work?

A

Competes with Vitamin K – complicated metabolism
Many dietary, physiological and drug interactions
Narrow therapeutic index and requires monitoring
Reduces production of functional coagulation factors
Induces an anticoagulated state slowly
Reversible

61
Q

How is the action of Warfarin reversed?

A

Reversed slowly by Vit K administration – takes several hours to work
Reversed rapidly by infusion of coagulation factors:
PCC (Prothrombin Complex Concentrate- contains Factors II, VII, IX and X)
FFP (Fresh Frozen Plasma)

62
Q

What are side effects of Warfarin?

A 
Bleeding
Minor 5% pa
Major 0.9 – 3.0% pa
Fatal 0.25% pa
Skin Necrosis
Purple toe syndrome
Embryopathy – Chondrodysplasia punctata
63
Q

What are the features of skin necrosis?

A

Skin Necrosis
Severe Protein C deficiency
2-3 days after starting Warfarin
Thrombosis predominantly in adipose tissues

64
Q

What are the features of purple toe syndrome?

A

Disrupted atheromatous plaques bleed

Cholesterol emboli lodge in extremities

65
Q

What is chondrodysplasia punctata?

A

Early fusion of epiphyses

Warfarin teratogenic in 1st trimester

66
Q

How do you monitor warfarin?

A

International Sensitivity Index
Indicates sensitivity of particular thromboplastin for warfarin
Unanticoagulated normal INR = 1.0
Target INR usually 2-3

67
Q

What can cause resistance to warfarin?

A

Lack of patient compliance

Measure warfarin levels

Proteins Induced by Vitamin K Absence (PIVKA)

Diet, Increased Vit K intake

Increased metabolism Cyt P450 (CYP2C9)

Reduced binding (VKORC1)

68
Q

What would you give for initial treatment to minimise clot extension (< 3 months)?

A

DOAC or LMWH for first few days followed by DOAC or warfarin

69
Q

What would you give for long term treatment to reduce risk of recurrence?

A

DOAC or warfarin

70
Q

What would you give for AF?

A

DOAC or warfarin

71
Q

What would you give for mechanical prosthetic heart valve?

A

Warfarin (DOACs not effective and should be avoided)

72
Q

What would you give following surgery?

A

LMWH or DOAC

73
Q

What would you give during pregnancy?

A

LMWH (DOACs not safe in pregnancy)

74
Q

How would you tip the balance towards venous thrombosis?

A

Decreased fibrinolytic factors
Decreased anticoagulant factors

Increase coagulant factors
Increase platelets

75
Q

How would you tip the balance towards

A

Increased fibrinolytic factors
Increased anticoagulant factors

Decrease coagulant factors
Decrease platelets

Year 2 Cardio (10 decks)

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